کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5896839 | 1568734 | 2016 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Blockade of TGF-β-activated kinase 1 prevents advanced glycation end products-induced inflammatory response in macrophages
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کلمات کلیدی
MCP-1MAP3K7TGF-β-activated kinase 1TAK1TABSIL-1βAGEsNF-κBBMMs - BMM هاMAPK - MAPKMAPKs - MAPK هاinflammation - التهاب( توروم) Interleukin-1 beta - اینترلوکین-1 بتاtumor necrosis factor-alpha - تومور نکروز عامل آلفاTNF-α - فاکتور نکروز توموری آلفاBone marrow-derived macrophages - ماکروفاژها حاصل از استخوان مغز استخوانAdvanced glycation end products - محصولات نهایی پیشرفته گلیساسیونBMP - مدیریت فرایند کسب و کارDiabetic nephropathy - نفروپاتی دیابتیmonocyte chemo-attractant protein-1 - پروتئین شیمیایی جذب مونوسیت-1Bone morphogenetic protein - پروتئین مورفوژنیک استخوانmitogen-activated protein kinases - کیناز پروتئین فعال Mitogen
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
علوم غدد
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چکیده انگلیسی
Advanced glycation end products (AGEs), inflammatory-activated macrophages are essential in the initiation and progression of diabetic nephropathy (DN). TGF-β-activated kinase 1 (TAK1) plays a vital role in innate immune responses and inflammation. However, little information has been available about the effects of AGEs on the regulation of TAK1 expression and underlying mechanisms in AGEs-stimulated macrophage activation. We hypothesized TAK1 signal pathway in AGEs conditions could be a vital factor contributing to macrophage activation and inflammation. Thus, in the present study, we used bone marrow-derived macrophages (BMMs) to explore the functional role and potential mechanisms of TAK1 pathway under AGEs conditions. Results indicated that TAK1 played important roles in AGEs-induced mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B protein (NF-κB) activation, which regulated the production of monocyte chemo-attractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) in AGEs-stimulated macrophages. The results also suggested that TAK1 inhibitor (5Z-7-oxozeaenol) could inhibit AGEs-induced macrophage activation to down-regulate inflammatory cytokine production via MAPKs and NF-κB pathways, indicating that 5Z-7-oxozeaenol might be an immunoregulatory agent against AGEs-stimulated inflammatory response in DN.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cytokine - Volume 78, February 2016, Pages 62-68
Journal: Cytokine - Volume 78, February 2016, Pages 62-68
نویسندگان
Xingxin Xu, Xiangming Qi, Yunxia Shao, Yuanyuan Li, Xin Fu, Shiyao Feng, Yonggui Wu,